ArticlePLoS pathogens2014
HMGB1-promoted and TLR2/4-dependent NK cell maturation and activation take part in rotavirus-induced murine biliary atresia.
Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 52 citations in OpenAlex.
- Role of HMGB1 in Neuroinflammation.Molecular neurobiology · 2026Review
- IL‑17AInternational journal of molecular medicine · 2026Article
- Defective efferocytosis in diabetes: molecular mechanisms and emerging therapeutic strategies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Rotavirus Reverse Genetics Systems and Oral Vaccine Delivery Vectors for Mucosal Vaccination.Microorganisms · 2025Review
- Vitamin D3/VDR alleviates double-stranded RNA virus -induced biliary epithelial cell damage by inhibiting autophagy.BMC gastroenterology · 2025Article
- NK cell function down regulated by HMGB2 through ANGPT1/PI3K/AKT pathway and its effect on esophageal squamous carcinoma cells.Frontiers in immunology · 2025Article
- Immunology of Biliary Atresia.Seminars in pediatric surgery · 2024Review
- High Mobility Group Box 1 and Cardiovascular Diseases: Study of Act and Connect.Cardiovascular toxicology · 2024Review
- Biliary atresia.Nature reviews. Disease primers · 2024Review
- The protective role of prebiotics and probiotics on diarrhea and gut damage in the rotavirus-infected piglets.Journal of animal science and biotechnology · 2024Review
- Role of cholinergic innervation in biliary remnants of patients with biliary atresia.Frontiers in pediatrics · 2023Article
- Editorial: Viruses and immune response in pediatric infection.Frontiers in cellular and infection microbiology · 2023Article
- Natural killer cells in sepsis: Friends or foes?Frontiers in immunology · 2023Review
- Review
- Current Understanding in the Clinical Characteristics and Molecular Mechanisms in Different Subtypes of Biliary Atresia.International journal of molecular sciences · 2022Review
- A joint transcriptional regulatory network and protein activity inference analysis identifies clinically associated master regulators for biliary atresia.Frontiers in pediatrics · 2022Article
- Genetic Factors and Their Role in the Pathogenesis of Biliary Atresia.Frontiers in pediatrics · 2022Review
- Review
- Down-regulation of STAT3 enhanced chemokine expression and neutrophil recruitment in biliary atresia.Clinical science (London, England : 1979) · 2021Article
- The performance of the alarmin HMGB1 in pediatric diseases: From lab to clinic.Immunity, inflammation and disease · 2021Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies show that NK cells play important roles in murine biliary atresia (BA), and a temporary immunological gap exists in this disease. In this study, we found high-mobility group box-1 (HMGB1) and TLRs were overexpressed in human and rotavirus-induced murine BA. The overexpressed HMGB1 released from the nuclei of rotavirus-infected cholangiocytes, as well as macrophages, activated hepatic NK cells via HMGB1-TLRs-MAPK signaling pathways. Immature NK cells had low cytotoxicity on rotavirus-injured cholangiocytes due to low expression of TLRs, which caused persistent rotavirus infection in bile ducts. HMGB1 up-regulated the levels of TLRs of NK cells and promoted NK cell activation in an age-dependent fashion. As NK cells gained increasing activation as mice aged, they gained increasing cytotoxicity on rotavirus-infected cholangiocytes, which finally caused BA. Adult NK cells eliminated rotavirus-infected cholangiocytes shortly after infection, which prevented persistent rotavirus infection in bile ducts. Moreover, adoptive transfer of mature NK cells prior to rotavirus infection decreased the incidence of BA in newborn mice. Thus, the dysfunction of newborn NK cells may, in part, participate in the immunological gap in the development of rotavirus induced murine BA.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.